Experiential feeling therapy addressing the pain of the lack of love.
“Truth needs no defense except when that truth is more than the system can integrate; then it requires defenses.
Our merciful brain has found back-up ways to protect us. It keeps the truth from us even when we go on searching for the truth.
After patients have deep feelings they come up with many truths about their lives. It is buried and defended along with the pain. Thus no one has to give anyone insights; they are already there just waiting for the exit.”
http://cigognenews.blogspot.com/2016/01/the-act-out-and-more_29.html “The Act-out and More”
Neuroskeptic’s blog post Genetic Testing for Autism as an Existential Question related “A Sister, a Father and a Son: Autism, Genetic Testing, and Impossible Decisions” story:
“I decided to put the question to my sister, Maria. Although she is autistic, she is of high intelligence.
Maria was excited to be an aunt soon, and was willing to do what she could to help my baby – even if what she was helping with was to avoid her own condition.
She is high enough functioning to know some of what she’s missing in life, and has longed her entire life to be “normal.” If she could save her niece or nephew some of the pain and awkwardness her condition had caused her, she was willing to help.”
In the concluding paragraph:
“What struck me about this story is the way in which the prospect of the genetic test confronted Maria with a very personal decision: will you do something that might help prevent someone else becoming like you?
Isn’t this very close to the ultimate existential question: all things considered, would you wish to live your life over again?”
Aren’t the majority of humans also “high enough functioning to know some of what she’s missing in life?”
Isn’t our feeling of what we’re missing one of the impetuses for us to have also “longed her entire life to be normal?”
This feeling was aired in Dr. Arthur Janov’s blog post What a Waste:
“What it was, was the feeling of great loss, something missing that could never again be duplicated.
It was no love where it could have been the opposite if the parent’s gates could have been open. But it could not be because that would have meant terrible pain and suffering for them; and their whole neurologic system militated against any conscious-awareness.”
We long for what was and is impossible:
- For many of us, the impossibilities of having normal lives started with prenatal epigenetic changes.
- Our experiences of our postnatal environment prompted us into adapting to its people, places, and contents. These neurological, biological, and behavioral adaptations were sometimes long-lasting deviations from developmental norms.
- Other genetic factors combined with the above to largely make us who we were and are.
Our longing for an impossible-to-reconstruct life doesn’t go away.
We may not be often aware of our longing for what “could not be” and of its extensive impacts. But such feelings impel us into so many thousands of ideas, beliefs, and behaviors, a sample of which were referred to above:
- Behaviors to “do something that might help prevent someone else becoming like you”
- Ideas such as existential philosophy
- Beliefs that manifest the “wish to live your life over again.”
The problem is that spending our time and efforts on these ideas, beliefs, and behaviors won’t ameliorate their motivating causes. Efforts so impelled only distance us further away from our truths, with real consequences: a wasted life.
What keeps an individual from understanding their reality? I invite readers to investigate Dr. Arthur Janov’s Primal Therapy for effective therapeutic approaches.
This 2015 US/Canadian human study of people ages 6 to 22 years found:
“Testosterone-specific associations between amygdala volume and key prefrontal areas involved in emotional regulation and impulse control:
- Testosterone-specific modulation of the covariance between the amygdala and medial prefrontal cortex (mPFC);
- A significant relationship between amygdala-mPFC covariance and levels of aggression; and
- Mediation effects of amygdala-mPFC covariance on the relationship between testosterone and aggression.
These effects were independent of sex, age, pubertal stage, estradiol levels and anxious-depressed symptoms.
For the great majority of individuals in this sample, higher thickness of the mPFC was associated with lower aggression levels at a given amygdala volume..this effect diminished greatly and disappeared at more extreme amygdala values.”
The study provided noncausal associations among the effects (behavioral, hormonal, and brain measurements).
From the Limitations section:
“No umbilical cord or amniotic measurements were available in this study and we therefore cannot control for testosterone levels in utero, a period during which significant testosterone-related changes in brain structure are thought to occur.”
There’s evidence that too much testosterone for a female fetus and too little testosterone for a male fetus both have lifelong adverse effects. The researchers dismissed this etiologic line of inquiry with a “supporting the notion” referral to noncausal studies.
The researchers were keen to establish:
“A very specific, aggression-related structural brain phenotype.”
This putative phenotype hinged on:
- Older subjects’ behavioral self-reports, and
- Parental assessments of younger subjects’ behavior
exhibited during the previous six months, and within six months of their fMRI scan.
These self-reports and interested-party observations were the entire bases for the “aggressive behavior” and “anxious–depressed” associations. The researchers provided multiple references and models for the reliability of these assessments.
Experimental behavioral measurements – such as those done to measure performance in decision studies – may have been more accurate and informative than what the older subjects chose to self-report about their own behavior over the previous six months.
People of all ages have an imperative to NOT be completely honest about their own behavior. One motivation for this condition is that some of our historical realities are too painful to enter our conscious awareness and inform us about our own behavior. As a result, our feelings, thoughts, and behavior are sometimes driven by our histories without us being aware of it.
For example, would a teenager/young adult subject self-report an impulsive act, even if they didn’t fully understand why they acted that way? Maybe they would if the act could be viewed as prosocial, but what if it was antisocial?
What are the chances that the lives of these teenager/young adult subjects were NOT filled with impulsive actions during the six months before their fMRI scans? Could complete and accurate self-reports of such behaviors be expected?
Experimental behavioral measurements may have also been more accurate and informative than second-hand, interested-party observations of the younger subjects. Could someone who provided half of the genes and who was responsible for many of their child’s epigenetic changes make anything other than subjective observations of their handiwork’s behavior?
Epigenetic studies have shown that adaptations to environments are among the long-lasting causes for effects that include behavior, hormones, and brain measurements. Why, in 2015, did researchers spend public funds developing what they knew or should have known would be noncausal associations, while not investigating possible causes for these effects?
Why weren’t the researchers interested enough to gather and assess etiologic genetic and epigenetic evidence? Was it that difficult to get blood samples at the same time the subjects gave saliva samples, and perform selected genetic and DNA methylation analyses?
What did the study contribute towards advancing science? Who did the study really help?
http://www.psyneuen-journal.com/article/S0306-4530%2815%2900924-5/fulltext “A testosterone-related structural brain phenotype predicts aggressive behavior from childhood to adulthood”
In this 2014 review, a social scientist first presented an interpretive history of what he found to be important in the emergence of epigenetics. He proceeded into his view of “a possible agenda of the social studies of the life-sciences” in the “postgenomic age” with headings such as “Postgenomic biopolitics: “upgrade yourself” or born damaged for ever?”
This view included:
“The upgradable epigenome may become the basis for a new motivation to intervene, control and improve it through pharmacological agents or social interventions.
An important trend is the use of epigenetic and developmental findings in the so-called early-intervention programmes.
It is possible that epigenetic findings will become increasingly relevant in social policy strategies.”
I work in Washington DC, a town that’s a magnet for people who want to exercise control over other people’s lives. Interventions in various forms are something I see and hear about every day.
In this blog I often highlight research that may help us understand details of how each of us is a unique individual. It’s my view that insofar as research helps each of us understand our unique, real self, we may be able to empathetically understand others’ unique qualities.
The same research may be viewed as a vehicle to promote opportunities for interventions into others’ lives. A clinical study is typically designed to test within defined parameters whether a specific intervention will be effective.
This approach may be counterproductive, though, when assessing epigenetic factors in “social studies of the life-sciences.” The researchers will note “individual differences” and then explain them away in order to converge on the desired objective. The researchers seldom attempt to further understand what caused each subject to develop their unique qualities.
Why would a person employed in the social sciences, their funders, and someone employed or involved in social services intentionally disregard an individual’s unique qualities? In my opinion, this reflexive action derives from a person being unable to face the facts of their own life.
Several relevant fundamentals of Dr Arthur Janov’s Primal Therapy are:
- Pain motivates a person’s unconscious act outs of their underlying problems.
- The behavior that caused a problem is sometimes also the act-out behavior.
- Act outs enable a person to re-experience the feelings of their historical struggles, in a vain attempt to resolve them.
- Due to pain barriers, people seldom become consciously aware of and – more importantly – address the causes for their problematic behavior.
- “The patient has the power to heal himself.”
A consequent hypothesis is that a person will often glorify their unconscious behavior and surround themself with justifications for it. For example, a person who can’t sit still may refer to their incessant activity with socially acceptable phrases such as “I’m always busy” or “I love to travel.” They’ll structure their life to enable their unconscious act outs, never questioning how they were attracted to an always-on-the-go occupation such as flight attendant, only vaguely feeling that they were made for it.
The behavior relevant to the current review may be exhibited by a person with a history of having no control over their own life. Following the above first two fundamentals, the pain of historically not having control over their life may motivate them to control other people’s lives.
Unfortunately for everyone who’s affected, such unconscious behavior doesn’t resolve anything:
- The initiator may achieve some symbolic satisfaction by controlling others’ lives.
- The temporary satisfaction doesn’t make the initiator’s underlying problems less painful.
- The motivation driving their unconscious act outs isn’t thereby reduced.
- The initiator repeats their controlling behavior, stuck in a loop of unresolved feelings.
- Since the self-chosen interests of someone who’s being controlled are lesser concerns to the initiator than control, the controlled person may or may not be helped by the controller’s act outs.
Research provides abundant evidence that we are unique individuals. To me, it’s a strong indicator of who’s best qualified to figure out what to do with each of our unique lives.
A person who’s driven to control others’ lives usually won’t accept research into epigenetics as instructive for understanding themself as an individual. They’ll unconsciously use research as a way to enable their act outs, and as such, view it as offering opportunities for interventions into the lives of others.
So “pharmacological agents or social interventions” are often the intended “use of epigenetic and developmental findings.” Interventions receive justifications with “a possible agenda of the social studies of the life-sciences.”
A person becoming aware of their own act outs, then individually addressing their own underlying problems, often take backseats to their employment and other concerns to keep enabling their behavior. That makes it likely that interventions justified by “epigenetic findings..in social policy” will continue, regardless of whether the subjects agree that they’re being helped.
For examples, take a look at a few of the presentations by people employed in the social sciences and social services on a topic of epigenetics. Compare them with the topic’s update to the current state of epigenetic research in Grokking an Adverse Childhood Experiences (ACE) score.
What did you notice? Did anyone emphasize disrupted prenatal development, a period when problems can be prevented? I saw that many more of the presentations emphasized controlling behavior.
http://journal.frontiersin.org/article/10.3389/fnhum.2014.00309/full “The social brain meets the reactive genome: neuroscience, epigenetics and the new social biology”
This 2015 French rodent study found:
“Memories can be established and maintained without de novo protein synthesis and that experimental amnesia may not result from a disruption of memory consolidation/reconsolidation.
Posttraining/postreactivation treatments induce an internal state, which becomes encoded with the memory, and should be present at the time of testing to ensure a successful retrieval.
This integration concept includes most of the previous explanations of memory recovery after retrograde amnesia and critically challenges the traditional memory consolidation/reconsolidation hypothesis, providing a more dynamic and flexible view of memory.”
From Neuroskeptic’s analysis of the study:
“A different drug, lithium chloride, produces the same pattern of effects – it blocks ‘reconsolidation’, but this can be reversed by a second dose at the time of recall. However, lithium chloride is not an amnestic [a drug that blocks memory formation] – it doesn’t block protein synthesis. Rather, it causes nausea.
The implication of the lithium experiment is that any drug that causes an ‘internal state change’, even if it’s just nausea, can trigger state-dependent memory and behave just like an ‘amnestic’.”
As this study may apply to humans, a drug wouldn’t necessarily be required to “induce an internal state.” If the findings of studies such as Are 50 Shades of Grey behaviors learned in infancy? extend to humans, an emotional or physical experience may be sufficient to produce a state-dependent memory. For example, A study that provided evidence for basic principles of Primal Therapy found, albeit with rodents and use of a drug:
“Fear-inducing memories can be state dependent, meaning that they can best be retrieved if the brain states at encoding and retrieval are similar.”
Memories triggered while in a brain state reentered through an emotion or a physical reaction are experienced by Primal Therapy patients and observed by therapists every day. However, as mentioned in What scientific evidence can be offered for Primal Therapy’s capability to benefit people’s lives? there’s a difficulty in developing human evidence for such state-dependent emotional memories.
Standard procedures would use human subjects and control groups in a way that retrieved memories according to the researchers’ schedule and experimental parameters. In order for the retrieval of an emotional memory to be therapeutic, though, the methods of an experiential therapy such as Dr. Arthur Janov’s Primal Therapy leave the timing of entering a triggering brain state up to the patient.
When a brain state protects a human emotional memory from being accessed, it probably wouldn’t be therapeutic to:
- Force a return to that brain state, and thereby
- Remove the memory’s protection, then
- Retrieve and re-experience the memory
just for the sake of research.
The evidence for retrieving and re-experiencing a state-dependent memory lies mainly within the individual’s experiences.
A challenge is to find innovative ways to document human evidence for state-dependent emotional memories while ensuring a therapeutic process.
http://www.jneurosci.org/content/35/33/11623 “Integration of New Information with Active Memory Accounts for Retrograde Amnesia: A Challenge to the Consolidation/Reconsolidation Hypothesis?”
This 2015 Northwestern rodent study found:
“Fear-inducing memories can be state dependent, meaning that they can best be retrieved if the brain states at encoding and retrieval are similar.
Memories formed in a particular mood, arousal or drug-induced state can best be retrieved when the brain is back in that state.
“It’s difficult for therapists to help these patients,” Radulovic said, “because the patients themselves can’t remember their traumatic experiences that are the root cause of their symptoms.”
The best way to access the memories in this system is to return the brain to the same state of consciousness as when the memory was encoded.”
The study demonstrated one method of activating neurobiological pathways with a drug to remove a hippocampal memory’s protection, which played a part in enabling the subjects to relive their remembered experiences. This rodent study wasn’t designed to address how to therapeutically access similarly protected memories with humans.
The study informed us with evidence for fundamentals of Dr. Arthur Janov’s Primal Therapy, such as:
- Experiences associated with pain can be remembered below our conscious awareness.
- The retrieval and re-experiencing of emotional memories can engage our lower-level brain areas without our higher-level brain areas’ participation.
From the Northwestern press release:
“There are two kinds of GABA [gamma-Aminobutyric acid] receptors. One kind, synaptic GABA receptors, works in tandem with glutamate receptors to balance the excitation of the brain in response to external events such as stress.
The other population, extra-synaptic GABA receptors, are independent agents.
If a traumatic event occurs when these extra-synaptic GABA receptors are activated, the memory of this event cannot be accessed unless these receptors are activated once again.
“It’s an entirely different system even at the genetic and molecular level than the one that encodes normal memories,” said lead study author Vladimir Jovasevic, who worked on the study when he was a postdoctoral fellow in Radulovic’s lab.
This different system is regulated by a small microRNA, miR-33, and may be the brain’s protective mechanism when an experience is overwhelmingly stressful.
The findings imply that in response to traumatic stress, some individuals, instead of activating the glutamate system to store memories, activate the extra-synaptic GABA system and form inaccessible traumatic memories.”
I’d point out that the “can’t remember” and “inaccessible traumatic memories” phrases used above were in reference to what’s usually called “memory” i.e., a recall initiated using the cerebrum. The study’s findings should inform researchers who perform memory studies involving the hippocampus if they care to understand how emotional memories can be formed and re-experienced.
The obvious nature of this study’s straightforward experimental methods made me wonder why other researchers hadn’t used the same methods decades ago. It could have resulted in dozens of informative follow-on study variations by now, and subsequently found whether the subjects’ physiological, behavioral, and genetic measurements differed from control group subjects, as in:
“miR-33 is downregulated in response to gaboxadol [the drug used to change the subjects’ brain state] and modulates its effects on state-dependent fear.“
http://www.nature.com/neuro/journal/v18/n9/full/nn.4084.html “GABAergic mechanisms regulated by miR-33 encode state-dependent fear”
MP3 with lead researcher Dr. Jelena Radulovic: http://www.thenakedscientists.com/HTML/specials/show/20150825/